Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz
Gewählte Publikation:
SHR Neuro Krebs Kardio Lipid Stoffw Microb
Semsroth, S; Fellner, B; Trescher, K; Bernecker, OY; Kalinowski, L; Gasser, H; Hallström, S; Malinski, T; Podesser, BK.
S-nitroso human serum albumin attenuates ischemia/reperfusion injury after cardioplegic arrest in isolated rabbit hearts.
J HEART LUNG TRANSPLANT. 2005; 24: 2226-2234.
Doi: 10.1016/j.healun.2005.08.004
Web of Science
PubMed
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- Co-Autor*innen der Med Uni Graz
- Hallström Seth
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- Abstract:
- Background: Depletion of nitric oxide (NO) is associated with ischemia/reperfusion injury. The novel NO donor, S-nitroso human serum albumin (S-NO-HSA), could bridge NO depletion during reperfusion in cardiac transplantation and minimize ischemia/reperfusion injury. Methods: In an isolated erythrocyte-perfused working heart model, rabbit hearts were randomly assigned after assessment of hemodynamic baseline values to receive S-NO-HSA (0.2 mu mol/100 ml, n = 8), L-arginine (10 mmol/100 ml, n = 8) or albumin (control) (0.2 mu mol/100 ml, n = 8). After 20 minutes of infusion, the hearts were arrested and stored in Celsior (4 degrees C) enriched with respective drugs for 6 hours, followed by 75 minutes of reperfusion. Hemodynamic values were assessed and biopsy specimens were taken to determine calcium-ionophore stimulated release of NO and superoxide. Results: During early reperfusion, recovery of cardiac output (75% +/- 6% vs 49% +/- 5%, P < 0.05) and coronary flow (99% +/- 8% vs 70% +/- 5%, P < 0.05) were higher, and myocardial oxygen consumption was reduced in the S-NO-HSA Group compared with Control (4.08 +/- 0.46 ml/min/0.1 kg vs 6.78 +/- 0.38 ml/min/0.1 kg, p < 0.01). At the end of the experiment cardiac output (53% +/- 5% vs 27% +/- 5%, P < 0.01) was higher and left atrial pressure (115% +/- 9% vs 150% +/- 8%, p < 0.05) was lower in the S-NO-HSA Group compared with Control. NO release was increased (1,040 +/- 50 nmol/liter and 1,070 +/- 60 nmol/liter vs 860 +/- 10 nmol/liter, p < 0.01) and superoxide release diminished (31 +/- 5 nmol/liter and 38 +/- 5 nmol/liter vs 64 +/- 5 nmol/liter, p < .01) in the S-NO-HSA and L-arginine Groups compared with Control. Conclusion: S-NO-HSA improved hemodynamic functions after prolonged hypothermic cardiac arrest by supplementing NO and thereby decreasing ischemia/reperfusion injury.
- Find related publications in this database (using NLM MeSH Indexing)
- Animals -
- Cardiac Output -
- Circulatory Arrest, Deep Hypothermia Induced - adverse effects
- Endothelium - drug effects
- Heart Transplantation - drug effects
- Hemodynamic Processes - drug effects
- Myocardium - metabolism
- Nitric Oxide - metabolism
- Nitroso Compounds - pharmacology
- Organ Preservation - methods
- Oxygen Consumption - methods
- Rabbits - methods
- Reperfusion Injury - physiopathology
- Research Support, Non-U.S. Gov't - physiopathology
- Serum Albumin - pharmacology